Although a linear definition of aging and its effects on diseases associated with oxidative stress, inflammation, and metabolic dysregulation has been elusive, the process of aging can be thought of as a stochastic process that systemically occurs in animals after reproductive maturity, resulting in a gradual increase in molecular disorder. As molecular fidelity decreases, the cell's ability to repair or replace molecular constituents becomes abrogated, leading to increased susceptibility to age-related diseases.
Interestingly, because aberrant cellular energetics (i.e. metabolic dysregulation) have been shown in several model organisms to determine lifespan and longevity, nearly all molecules, including those that orchestrate cellular repair and replacement, must be subject to the same stochastic process that potentiates molecular disorder and decreases fidelity. Indeed, such molecules must have existed at one point in time (before reproductive maturity) without any changes associated with the process of aging.
Thus, because aging is an imbalance between cellular damage and repair, researchers have focused on the etiological players of cellular damage and have highlighted three wide-ranging pathological states that have been associated with the origin of numerous age-related and non-age related disease states: (1) oxidative stress; (2) inflammation; and (3) metabolic dysregulation (i.e. mitochondrial dysfunction).